Damage to an allograft can continue for years after transplantation, and despite improvements in immunosuppressive drugs and organ preservation, chronic rejection is still the most important factor in the failure of transplanted grafts .. Histologically, during chronic rejection, smooth muscle cells are seen to proliferate in the vasculature of the transplanted organ, sometimes resulting in transplant atherosclerosis; several factors can contribute to this end point. Adhesion molecules such as intercellular adhesion molecule 1 (ICAM-1 or CD54; and growth factors such as vascular endothelial-cell growth factor are upregulated, and inducible nitric oxide synthase is imbalanced ..
ICAM-1
ICAM-1 is a member of the Ig superfamily and is very important in both cellular adhesion and T-cell co-stimulation. Strategies to reduce T-cell activation by eliminating the effects of ICAM-1 have been carried out successfully in clinical trials involving renal allograft patients and the use of antibodies targeted against the ICAM-1 molecule.. In a study of 18 patients, the anti-ICAM-1 antibody (BIRR1) was given to those patients who had received renal grafts from cadaver donors and were at a high risk for delayed graft function. An adequate level of BIRR1 in the serum (>10 mg/ml) was found to significantly reduce the incidence of both delayed graft function (p<0.01)>
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